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The interferon response circuit: Induction and suppression by pathogenic viruses
Type I interferons (IFN-α/β) are potent antiviral cytokines and modulators of the adaptive immune system. They are induced by viral infection or by double-stranded RNA (dsRNA), a by-product of viral replication, and lead to the production of a broad range of antiviral proteins and immunoactive cytok...
Autores principales: | , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Elsevier Inc.
2006
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7125643/ https://www.ncbi.nlm.nih.gov/pubmed/16364743 http://dx.doi.org/10.1016/j.virol.2005.09.024 |
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author | Haller, Otto Kochs, Georg Weber, Friedemann |
author_facet | Haller, Otto Kochs, Georg Weber, Friedemann |
author_sort | Haller, Otto |
collection | PubMed |
description | Type I interferons (IFN-α/β) are potent antiviral cytokines and modulators of the adaptive immune system. They are induced by viral infection or by double-stranded RNA (dsRNA), a by-product of viral replication, and lead to the production of a broad range of antiviral proteins and immunoactive cytokines. Viruses, in turn, have evolved multiple strategies to counter the IFN system which would otherwise stop virus growth early in infection. Here we discuss the current view on the balancing act between virus-induced IFN responses and the viral counterplayers. |
format | Online Article Text |
id | pubmed-7125643 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2006 |
publisher | Elsevier Inc. |
record_format | MEDLINE/PubMed |
spelling | pubmed-71256432020-04-08 The interferon response circuit: Induction and suppression by pathogenic viruses Haller, Otto Kochs, Georg Weber, Friedemann Virology Article Type I interferons (IFN-α/β) are potent antiviral cytokines and modulators of the adaptive immune system. They are induced by viral infection or by double-stranded RNA (dsRNA), a by-product of viral replication, and lead to the production of a broad range of antiviral proteins and immunoactive cytokines. Viruses, in turn, have evolved multiple strategies to counter the IFN system which would otherwise stop virus growth early in infection. Here we discuss the current view on the balancing act between virus-induced IFN responses and the viral counterplayers. Elsevier Inc. 2006-01-05 2005-12-16 /pmc/articles/PMC7125643/ /pubmed/16364743 http://dx.doi.org/10.1016/j.virol.2005.09.024 Text en Copyright © 2005 Elsevier Inc. All rights reserved. Since January 2020 Elsevier has created a COVID-19 resource centre with free information in English and Mandarin on the novel coronavirus COVID-19. The COVID-19 resource centre is hosted on Elsevier Connect, the company's public news and information website. Elsevier hereby grants permission to make all its COVID-19-related research that is available on the COVID-19 resource centre - including this research content - immediately available in PubMed Central and other publicly funded repositories, such as the WHO COVID database with rights for unrestricted research re-use and analyses in any form or by any means with acknowledgement of the original source. These permissions are granted for free by Elsevier for as long as the COVID-19 resource centre remains active. |
spellingShingle | Article Haller, Otto Kochs, Georg Weber, Friedemann The interferon response circuit: Induction and suppression by pathogenic viruses |
title | The interferon response circuit: Induction and suppression by pathogenic viruses |
title_full | The interferon response circuit: Induction and suppression by pathogenic viruses |
title_fullStr | The interferon response circuit: Induction and suppression by pathogenic viruses |
title_full_unstemmed | The interferon response circuit: Induction and suppression by pathogenic viruses |
title_short | The interferon response circuit: Induction and suppression by pathogenic viruses |
title_sort | interferon response circuit: induction and suppression by pathogenic viruses |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7125643/ https://www.ncbi.nlm.nih.gov/pubmed/16364743 http://dx.doi.org/10.1016/j.virol.2005.09.024 |
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